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Targeting Metabolism for Cancer Prevention and Therapy: Dietary and Pharmacological Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 3036

Special Issue Editor


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Guest Editor
Department of Pharmacology, Faculty of Pharmacy, University of Seville, 41012 Sevilla, Spain
Interests: phytochemicals; polyphenols; cancer; antioxidant; pro-oxidant; DNA damage; dietary supplements; signaling pathways; epigenetic; metabolism; immune system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In addition to developing DNA alterations, cancer cells reprogram their metabolism to meet their elevated energy demands, to produce building blocks for biosynthesis and proliferation, to survive under conditions of elevated oxidative stress, and to evade the immune system. The metabolic differences between cancer cells and normal cells offer an opportunity to develop new strategies to prevent and treat the disease.

The aim of this Special Issue is to collect original research and review articles on dietary and pharmacological approaches to target the metabolism for cancer prevention and therapy.

Dr. Estefanía Burgos-Morón
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer

  • metabolism
  • nutrients
  • amino acids
  • lipids
  • fatty acids
  • minerals
  • fasting
  • diet
  • drug
  • chemotherapy

Published Papers (2 papers)

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Research

19 pages, 4796 KiB  
Article
Gene and lncRNA Profiling of ω3/ω6 Polyunsaturated Fatty Acid-Exposed Human Visceral Adipocytes Uncovers Different Responses in Healthy Lean, Obese and Colorectal Cancer-Affected Individuals
by Sabrina Tait, Enrica Calura, Antonella Baldassarre, Andrea Masotti, Barbara Varano, Sandra Gessani, Lucia Conti and Manuela Del Cornò
Int. J. Mol. Sci. 2024, 25(6), 3357; https://doi.org/10.3390/ijms25063357 - 15 Mar 2024
Viewed by 639
Abstract
Colorectal cancer (CRC) is a major life-threatening disease, being the third most common cancer and a leading cause of death worldwide. Enhanced adiposity, particularly visceral fat, is a major risk factor for CRC, and obesity-associated alterations in metabolic, inflammatory and immune profiles in [...] Read more.
Colorectal cancer (CRC) is a major life-threatening disease, being the third most common cancer and a leading cause of death worldwide. Enhanced adiposity, particularly visceral fat, is a major risk factor for CRC, and obesity-associated alterations in metabolic, inflammatory and immune profiles in visceral adipose tissue (VAT) strongly contribute to promoting or sustaining intestinal carcinogenesis. The role of diet and nutrition in obesity and CRC has been extensively demonstrated, and AT represents the main place where diet-induced signals are integrated. Among the factors introduced with diet and processed or enriched in AT, ω3/ω6 polyunsaturated fatty acids (PUFAs) are endowed with pro- or anti-inflammatory properties and have been shown to exert either promoting or protective roles in CRC. In this study, we investigated the impact of ex vivo exposure to the ω3 and ω6 PUFAs docosahexaenoic and arachidonic acids on VAT adipocyte whole transcription in healthy lean, obese and CRC-affected individuals. High-throughput sequencing of protein-coding and long non-coding RNAs allowed us to identify specific pathways and regulatory circuits controlled by PUFAs and highlighted an impaired responsiveness of obese and CRC-affected individuals as compared to the strong response observed in healthy lean subjects. This further supports the role of healthy diets and balanced ω3/ω6 PUFA intake in the primary prevention of obesity and cancer. Full article
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19 pages, 7497 KiB  
Article
A Ketogenic Diet in Combination with Gemcitabine Mitigates Pancreatic Cancer-Associated Cachexia in Male and Female KPC Mice
by Natalia E. Cortez, Suraj Pathak, Cecilia Rodriguez Lanzi, Brian V. Hong, Ryman Crone, Rasheed Sule, Fangyi Wang, Shuai Chen, Aldrin V. Gomes, Keith Baar and Gerardo G. Mackenzie
Int. J. Mol. Sci. 2023, 24(13), 10753; https://doi.org/10.3390/ijms241310753 - 28 Jun 2023
Cited by 3 | Viewed by 1889
Abstract
Cancer-associated cachexia (CAC) is a critical contributor to pancreatic ductal adenocarcinoma (PDAC) mortality. Thus, there is an urgent need for new strategies to mitigate PDAC-associated cachexia; and the exploration of dietary interventions is a critical component. We previously observed that a ketogenic diet [...] Read more.
Cancer-associated cachexia (CAC) is a critical contributor to pancreatic ductal adenocarcinoma (PDAC) mortality. Thus, there is an urgent need for new strategies to mitigate PDAC-associated cachexia; and the exploration of dietary interventions is a critical component. We previously observed that a ketogenic diet (KD) combined with gemcitabine enhances overall survival in the autochthonous LSL-KrasG12D/+; LSL-Trp53 R172H/+; Pdx1-Cre (KPC) mouse model. In this study, we investigated the effect and cellular mechanisms of a KD in combination with gemcitabine on the maintenance of skeletal muscle mass in KPC mice. For this purpose, male and female pancreatic tumor-bearing KPC mice were allocated to a control diet (CD), a KD, a CD + gemcitabine (CG), or a KD + gemcitabine (KG) group. We observed that a KD or a KG-mitigated muscle strength declined over time and presented higher gastrocnemius weights compared CD-fed mice. Mechanistically, we observed sex-dependent effects of KG treatment, including the inhibition of autophagy, and increased phosphorylation levels of eIF2α in KG-treated KPC mice when compared to CG-treated mice. Our data suggest that a KG results in preservation of skeletal muscle mass. Additional research is warranted to explore whether this diet-treatment combination can be clinically effective in combating CAC in PDAC patients. Full article
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